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Abeta Peptide and Alzheimer’s Disease pp 198–215Cite as

Impact of β-Amyloid on the Tau Pathology in Tau Transgenic Mouse and Tissue Culture Models

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Abstract

Dementia is a generic term that describes chronic or progressive dysfunction of cortical and subcortical functions that result in complex cognitive decline. These cognitive changes are commonly accompanied by disturbances of mood, behavior, and personality. In developed countries with an increasingly aging population, the prevalence of dementia is currently at around 1.5% at 65 years of age, which doubles every 4 years and reaches about 30% at the age of 80 [1].

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References

  1. Ritchie K, Lovestone S. The dementias. Lancet 2002; 360:1759–66.

    PubMed  Google Scholar 

  2. Arnold SE, Hyman BT, Flory J, et al. The topographical and neuroanatomical distribution of neurofibrillary tangles and neuritic plaques in the cerebral cortex of patients with Alzheimer’s disease. Cereb Cortex 1991; 1:103–16.

    PubMed  CAS  Google Scholar 

  3. Ratnavalli E, Brayne C, Dawson K, Hodges JR. The prevalence of frontotemporal dementia. Neurology 2002; 58:1615–21.

    PubMed  CAS  Google Scholar 

  4. Kurosinski P, Guggisberg M, Gotz J. Alzheimer’s and Parkinson’s disease-Overlapping or synergistic pathologies? Trends Mol Med 2002; 8:3–5.

    PubMed  CAS  Google Scholar 

  5. Gotz J, Streffer JR, David D, et al. Transgenic animal models of Alzheimer’s disease and related disorders: Histopathology, behavior and therapy. Mol Psychiatry 2004; 9:664–683.

    PubMed  CAS  Google Scholar 

  6. Glenner GG, Wong CW. Alzheimer’s disease: initial report of the purification and characterization of a novel cerebrovascular amyloid protein. Biochem Biophys Res Commun 1984; 120:885–90.

    PubMed  CAS  Google Scholar 

  7. Masters CL, Simms G, Weinman NA, et al. Amyloid plaque core protein in Alzheimer’s disease and Down syndrome. Proc Natl Acad Sci U S A 1985; 82:4245–9.

    PubMed  CAS  Google Scholar 

  8. Vassar R, Bennett BD, Babu-Khan S, et al. Beta-secretase cleavage of Alzheimer’s amyloid precursor protein by the transmembrane aspartic protease BACE. Science 1999; 286:735–41.

    PubMed  CAS  Google Scholar 

  9. Edbauer D, Winkler E, Regula JT, et al. Reconstitution of gamma-secretase activity. Nat Cell Biol 2003; 5:486–8.

    PubMed  CAS  Google Scholar 

  10. Braak H, Braak E. Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol (Berlin) 1991; 82:239–59.

    CAS  Google Scholar 

  11. Braak H, Braak E. Staging of Alzheimer’s diseaserelated neurofibrillary changes. Neurobiol Aging 1995; 16:271–8; discussion 278-84.

    PubMed  CAS  Google Scholar 

  12. Crowther RA, Wischik CM. Image reconstruction of the Alzheimer paired helical filament. EMBO J 1985; 4:3661–5.

    PubMed  CAS  Google Scholar 

  13. Wischik CM, Crowther RA, Stewart M, Roth M. Subunit structure of paired helical filaments in Alzheimer’s disease. J Cell Biol 1985; 100:1905–12.

    PubMed  CAS  Google Scholar 

  14. Goedert M, Wischik CM, Crowther RA, et al. Cloning and sequencing of the cDNA encoding a core protein of the paired helical filament of Alzheimer’s disease: identification as the microtubuleassociated protein tau. Proc Natl Acad Sci U S A 1988; 85:4051–5.

    PubMed  CAS  Google Scholar 

  15. Lichtenberg B, Mandelkow EM, Hagestedt T, Mandelkow E. Structure and elasticity of microtubuleassociated protein tau. Nature 1988; 334:359–62.

    PubMed  CAS  Google Scholar 

  16. Schweers O, Schonbrunn-Hanebeck E, Marx A, Mandelkow E. Structural studies of tau protein and Alzheimer paired helical filaments show no evidence for beta-structure. J Biol Chem 1994; 269:24290–7.

    PubMed  CAS  Google Scholar 

  17. Goedert M, Spillantini MG, Jakes R, et al. Molecular dissection of the paired helical filament. Neurobiol Aging 1995; 16:325–34.

    PubMed  CAS  Google Scholar 

  18. Buee L, Bussiere T, Buee-Scherrer V, et al. Tau protein isoforms, phosphorylation and role in neurodegenerative disorders. Brain Res Brain Res Rev 2000; 33:95–130.

    PubMed  CAS  Google Scholar 

  19. Lee VM, Goedert M, Trojanowski JQ. Neurodegenerative tauopathies. Annu Rev Neurosci 2001; 24:1121–59.

    PubMed  CAS  Google Scholar 

  20. Gotz J. Tau and transgenic animal models. Brain Res Brain Res Rev 2001; 35:266–86.

    PubMed  CAS  Google Scholar 

  21. Chen F, David D, Ferrari A, Gotz J. Posttranslational modifications of tau-Role in human tauopathies and modeling in transgenic animals. Curr Drug Targets 2004; 5:503–15.

    PubMed  CAS  Google Scholar 

  22. Berriman J, Serpell LC, Oberg KA, et al. Tau filaments from human brain and from in vitro assembly of recombinant protein show cross-beta structure. Proc Natl Acad Sci U S A 2003; 100:9034–8.

    PubMed  CAS  Google Scholar 

  23. Goedert M, Jakes R. Mutations causing neurodegenerative tauopathies. Biochim Biophys Acta 2005; 1739:240–50.

    PubMed  CAS  Google Scholar 

  24. Tashiro K, Hasegawa M, Ihara Y, Iwatsubo T. Somatodendritic localization of phosphorylated tau in neonatal and adult rat cerebral cortex. Neuroreport 1997; 8:2797–801.

    PubMed  CAS  Google Scholar 

  25. Lee G, Rook SL. Expression of tau protein in nonneuronal cells: Microtubule binding and stabilization. J Cell Sci 1992; 102:227–37.

    PubMed  CAS  Google Scholar 

  26. Reszka AA, Seger R, Diltz CD, et al. Association of mitogen-activated protein kinase with the microtubule cytoskeleton. Proc Natl Acad Sci U S A 1995; 92:8881–5.

    PubMed  CAS  Google Scholar 

  27. Morishima-Kawashima M, Kosik KS. The pool of map kinase associated with microtubules is small but constitutively active.Mol Biol Cell 1996; 7:893–905.

    PubMed  CAS  Google Scholar 

  28. Flanagan LA, Cunningham CC, Chen J, et al. The structure of divalent cation-induced aggregates of PIP2 and their alteration by gelsolin and tau. Biophys J 1997; 73:1440–7.

    PubMed  CAS  Google Scholar 

  29. Ebneth A, Godemann R, Stamer K, et al. Overexpression of tau protein inhibits kinesindependent trafficking of vesicles, mitochondria, and endoplasmic reticulum: Implications for Alzheimer’s disease. J Cell Biol 1998; 143:777–94.

    PubMed  CAS  Google Scholar 

  30. Jenkins SM, Johnson GV. Tau complexes with phospholipase C-gamma in situ. Neuroreport 1998; 9:67–71.

    Article  PubMed  CAS  Google Scholar 

  31. Sontag E, Nunbhakdi-Craig V, Lee G, et al. Molecular interactions among protein phosphatase 2A, tau, and microtubules. Implications for the regulation of tau phosphorylation and the development of tauopathies. J Biol Chem 1999; 274:25490–8.

    PubMed  CAS  Google Scholar 

  32. Anderton BH, Dayanandan R, Killick R, Lovestone S. Does dysregulation of the Notch and wingless/ Wnt pathways underlie the pathogenesis of Alzheimer’s disease? Mol Med Today 2000; 6:54–9.

    PubMed  CAS  Google Scholar 

  33. De F, Gv, Inestrosa NC.Wnt signaling function in Alzheimer’s disease [In Process Citation]. Brain Res Brain Res Rev 2000; 33:1–12.

    Google Scholar 

  34. Maas T, Eidenmuller J, Brandt R. Interaction of tau with the neural membrane cortex is regulated by phosphorylation at sites that are modified in paired helical filaments. J Biol Chem 2000; 275:15733–40.

    PubMed  CAS  Google Scholar 

  35. Goedert M, Spillantini MG, Cairns NJ, Crowther RA. Tau proteins of Alzheimer paired helical filaments: abnormal phosphorylation of all six brain isoforms. Neuron 1992; 8:159–68.

    PubMed  CAS  Google Scholar 

  36. Sherrington R, Rogaev EI, Liang Y, et al. Cloning of a gene bearing missense mutations in early-onset familial Alzheimer’s disease. Nature 1995; 375:754–60.

    PubMed  CAS  Google Scholar 

  37. Van Broeckhoven C, Backhovens H, Cruts M, et al. Mapping of a gene predisposing to early-onset Alzheimer’s disease to chromosome 14q24.3. Nat Genet 1992; 2:335–9.

    PubMed  Google Scholar 

  38. Rocchi A, Pellegrini S, Siciliano G, Murri L. Causative and susceptibility genes for Alzheimer’s disease: A review. Brain Res Bull 2003; 61:1–24.

    PubMed  CAS  Google Scholar 

  39. Hodges JR, Davies RR, Xuereb JH, et al. Clinicopathological correlates in frontotemporal dementia. Ann Neurol 2004; 56:399–406.

    PubMed  Google Scholar 

  40. Dickson DW. Pick’s disease: A modern approach. Brain Pathol 1998; 8:339–54.

    Article  PubMed  CAS  Google Scholar 

  41. McKhann GM, Albert MS, Grossman M, et al. Clinical and pathological diagnosis of frontotemporal dementia: Report of the Work Group on Frontotemporal Dementia and Pick’s Disease. Arch Neurol 2001; 58:1803–9.

    PubMed  CAS  Google Scholar 

  42. Hodges JR, Davies R, Xuereb J, et al. Survival in frontotemporal dementia. Neurology 2003; 61:349–54.

    PubMed  CAS  Google Scholar 

  43. Hutton M, Lendon CL, Rizzu P, et al. Association of missense and 5-splice-site mutations in tau with the inherited dementia FTDP-17. Nature 1998; 393:702–5.

    PubMed  CAS  Google Scholar 

  44. Poorkaj P, Bird TD, Wijsman E, et al. Tau is a candidate gene for chromosome 17 frontotemporal dementia. Ann Neurol 1998; 43:815–25.

    PubMed  CAS  Google Scholar 

  45. Spillantini MG, Murrell JR, Goedert M, et al. Mutation in the tau gene in familial multiple system tauopathy with presenile dementia. Proc Natl Acad Sci U S A 1998; 95:7737–41.

    PubMed  CAS  Google Scholar 

  46. Clark LN, Poorkaj P, Wszolek Z, et al. Pathogenic implications of mutations in the tau gene in pallidoponto-nigral degeneration and related neurodegenerative disorders linked to chromosome 17. Proc Natl Acad Sci U S A 1998; 95:13103–7.

    PubMed  CAS  Google Scholar 

  47. Dumanchin C, Camuzat A, Campion D, et al. Segregation of a missense mutation in the microtubule-associated protein tau gene with familial frontotemporal dementia and parkinsonism. Hum Mol Genet 1998; 7:1825–9.

    PubMed  CAS  Google Scholar 

  48. Spillantini MG, Crowther RA, Kamphorst W, et al. Tau pathology in two Dutch families with mutations in the microtubule-binding region of tau. Am J Pathol 1998; 153:1359–63.

    PubMed  CAS  Google Scholar 

  49. Delisle MB, Murrell JR, Richardson R, et al. A mutation at codon 279 (N279K) in exon 10 of the Tau gene causes a tauopathy with dementia and supranuclear palsy. Acta Neuropathol (Berlin) 1999; 98:62–77.

    CAS  Google Scholar 

  50. D’Souza I, Poorkaj P, Hong M, et al. Missense and silent tau gene mutations cause frontotemporal dementia with parkinsonism-chromosome 17 type, by affecting multiple alternative RNA splicing regulatory elements. Proc Natl Acad Sci U S A 1999; 96:5598–603.

    PubMed  CAS  Google Scholar 

  51. Goedert M, Spillantini MG, Crowther RA, et al. Tau gene mutation in familial progressive subcortical gliosis. Nat Med 1999; 5:454–7.

    PubMed  CAS  Google Scholar 

  52. Mirra SS, Murrell JR, Gearing M, et al. Tau pathology in a family with dementia and a P301L mutation in tau. J Neuropathol Exp Neurol 1999; 58:335–45.

    PubMed  CAS  Google Scholar 

  53. Rizzu P, Van Swieten JC, Joosse M, et al. High prevalence of mutations in the microtubule-associated protein tau in a population study of frontotemporal dementia in the Netherlands. Am J Hum Genet 1999; 64:414–21.

    PubMed  CAS  Google Scholar 

  54. Sperfeld AD, Collatz MB, Baier H, et al. FTDP-17: An early-onset phenotype with parkinsonism and epileptic seizures caused by a novel mutation [see comments]. Ann Neurol 1999; 46:708–15.

    PubMed  CAS  Google Scholar 

  55. Arima K, Kowalska A, Hasegawa M, et al. Two brothers with frontotemporal dementia and parkinsonism with an N279K mutation of the tau gene. Neurology 2000; 54:1787–95.

    PubMed  CAS  Google Scholar 

  56. Delisle MB, Uro-Coste E, Murrell JR, et al. Neurodegenerative disease associated with a mutation of codon 279(N279K) in exon 10 of Tau protein. Bull Acad Natl Med 2000; 184:799–809.

    PubMed  CAS  Google Scholar 

  57. Tolnay M, Grazia Spillantini M, Rizzini C, et al. A new case of frontotemporal dementia and parkinsonism resulting from an intron 10 +3-splice site mutation in the tau gene: Clinical and pathological features. Neuropathol Appl Neurobiol 2000; 26:368–78.

    PubMed  CAS  Google Scholar 

  58. Lippa CF, Zhukareva V, Kawarai T, et al. Frontotemporal dementia with novel tau pathology and a Glu342Val tau mutation. Ann Neurol 2000; 48:850–8.

    PubMed  CAS  Google Scholar 

  59. Pastor P, Pastor E, Carnero C, et al. Familial atypical progressive supranuclear palsy associated with homozigosity for the delN296 mutation in the tau gene. Ann Neurol 2001; 49:263–7.

    PubMed  CAS  Google Scholar 

  60. Hayashi S, Toyoshima Y, Hasegawa M, et al. Late-onset frontotemporal dementia with a novel exon 1 (Arg5His) tau gene mutation. Ann Neurol 2002; 51:525–30.

    PubMed  CAS  Google Scholar 

  61. Goedert M, Crowther RA, Spillantini MG. Tau mutations cause frontotemporal dementias. Neuron 1998; 21:955–8.

    PubMed  CAS  Google Scholar 

  62. Delacourte A, Sergeant N, Wattez A, et al. Vulnerable neuronal subsets in Alzheimer’s and Pick’s disease are distinguished by their tau isoform distribution and phosphorylation. Ann Neurol 1998; 43:193–204.

    PubMed  CAS  Google Scholar 

  63. Mott RT, Dickson DW, Trojanowski JQ, et al. Neuropathologic, biochemical, and molecular characterization of the frontotemporal dementias. J Neuropathol Exp Neurol 2005; 64:420–8.

    PubMed  CAS  Google Scholar 

  64. Kurosinski P, Gotz J. Glial cells under physiologic and pathological conditions. Arch Neurol 2002; 59: 1524–8.

    PubMed  Google Scholar 

  65. Cervos-Navarro J, Schumacher K. Neurofibrillary pathology in progressive supranuclear palsy (PSP). J Neural Transm Suppl 1994; 42:153–64.

    PubMed  CAS  Google Scholar 

  66. Delacourte A. Pathological Tau proteins of Alzheimer’s disease as a biochemical marker of neurofibrillary degeneration. Biomed Pharmacother 1994; 48:287–95.

    PubMed  CAS  Google Scholar 

  67. Ksiezak-Reding H, Morgan K, Mattiace LA, et al. Ultrastructure and biochemical composition of paired helical filaments in corticobasal degeneration. Am J Pathol 1994; 145:1496–508.

    PubMed  CAS  Google Scholar 

  68. Wischik CM, Novak M, Thogersen HC, et al. Isolation of a fragment of tau derived from the core of the paired helical filament of Alzheimer’s disease. Proc Natl Acad Sci U S A 1988; 85:4506–10.

    PubMed  CAS  Google Scholar 

  69. Bondareff W, Wischik CM, Novak M, et al. Molecular analysis of neurofibrillary degeneration in Alzheimer’s disease. An immunohistochemical study. Am J Pathol 1990; 137:711–23.

    PubMed  CAS  Google Scholar 

  70. Murrell JR, Spillantini MG, Zolo P, et al. Tau gene mutation G389R causes a tauopathy with abundant pick body-like inclusions and axonal deposits. J Neuropathol Exp Neurol 1999; 58:1207–26.

    PubMed  CAS  Google Scholar 

  71. Rizzini C, Goedert M, Hodges JR, et al. Tau gene mutation K257T causes a tauopathy similar to Pick’s disease. J Neuropathol Exp Neurol 2000; 59:990–1001.

    PubMed  CAS  Google Scholar 

  72. Neumann M, Schulz-Schaeffer W, Crowther RA, et al. Pick’s disease associated with the novel Tau gene mutation K369I. Ann Neurol 2001; 50: 503–13.

    PubMed  CAS  Google Scholar 

  73. Rosso SM, van Herpen E, Deelen W, et al. A novel tau mutation, S320F, causes a tauopathy with inclusions similar to those in Pick’s disease. Ann Neurol 2002; 51:373–6.

    PubMed  CAS  Google Scholar 

  74. Kobayashi T, Ota S, Tanaka K, et al. A novel L266V mutation of the tau gene causes frontotemporal dementia with a unique tau pathology. Ann Neurol 2003; 53:133–7.

    PubMed  CAS  Google Scholar 

  75. van Herpen E, Rosso SM, Serverijnen LA, et al. Variable phenotypic expression and extensive tau pathology in two families with the novel tau mutation L315R. Ann Neurol 2003; 54:573–81.

    PubMed  Google Scholar 

  76. Pickering-Brown SM, Baker M, Nonaka T, et al. Frontotemporal dementia with Pick-type histology associated with Q336R mutation in the tau gene. Brain 2004; 127:1415–26.

    PubMed  CAS  Google Scholar 

  77. Stanford PM, Halliday GM, Brooks WS, et al. Progressive supranuclear palsy pathology caused by a novel silent mutation in exon 10 of the tau gene: expansion of the disease phenotype caused by tau gene mutations. Brain 2000; 123(Pt 5):880–93.

    PubMed  Google Scholar 

  78. Poorkaj P, Muma NA, Zhukareva V, et al. An R5L tau mutation in a subject with a progressive supranuclear palsy phenotype. Ann Neurol 2002; 52:511–6.

    PubMed  Google Scholar 

  79. Morris HR, Osaki Y, Holton J, et al. Tau exon 10 + 16 mutation FTDP-17 presenting clinically as sporadic young onset PSP. Neurology 2003; 61:102–4.

    PubMed  CAS  Google Scholar 

  80. Bugiani O, Murrell JR, Giaccone G, et al. Frontotemporal dementia and corticobasal degeneration in a family with a P301S mutation in tau. J Neuropathol Exp Neurol 1999; 58:667–77.

    PubMed  CAS  Google Scholar 

  81. Spillantini MG, Yoshida H, Rizzini C, et al. A novel tau mutation (N296N) in familial dementia with swollen achromatic neurons and corticobasal inclusion bodies. Ann Neurol 2000; 48:939–43.

    PubMed  CAS  Google Scholar 

  82. Thal DR, Rub U, Orantes M, Braak H. Phases of A beta-deposition in the human brain and its relevance for the development of AD. Neurology 2002; 58:1791–800.

    PubMed  Google Scholar 

  83. Crystal H, Dickson D, Fuld P, et al. Clinico-pathologic studies in dementia: nondemented subjects with pathologically confirmed Alzheimer’s disease. Neurology 1988; 38:1682–7.

    PubMed  CAS  Google Scholar 

  84. Arriagada PV, Growdon JH, Hedley-Whyte ET, Hyman BT. Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer’s disease. Neurology 1992; 42:631–9.

    PubMed  CAS  Google Scholar 

  85. Bierer LM, Hof PR, Purohit DP, et al. Neocortical neurofibrillary tangles correlate with dementia severity in Alzheimer’s disease. Arch Neurol 1995; 52:81–8.

    PubMed  CAS  Google Scholar 

  86. Nagy Z, Jobst KA, Esiri MM, et al. Hippocampal pathology reflects memory deficit and brain imaging measurements in Alzheimer’s disease: clinicopathologic correlations using three sets of pathologic diagnostic criteria. Dementia 1996; 7:76–81.

    PubMed  CAS  Google Scholar 

  87. Giannakopoulos P, Herrmann FR, Bussiere T, et al. Tangle and neuron numbers, but not amyloid load, predict cognitive status in Alzheimer’s disease. Neurology 2003; 60:1495–500.

    PubMed  CAS  Google Scholar 

  88. Delacourte A, David JP, Sergeant N, et al. The biochemical pathway of neurofibrillary degeneration in aging and Alzheimer’s disease [see comments]. Neurology 1999; 52:1158–65.

    PubMed  CAS  Google Scholar 

  89. Delacourte A, Sergeant N, Champain D, et al. Nonoverlapping but synergetic tau and APP pathologies in sporadic Alzheimer’s disease. Neurology 2002; 59:398–407.

    PubMed  CAS  Google Scholar 

  90. Caughey B, Lansbury PT. Protofibrils, pores, fibrils, and neurodegeneration: separating the responsible protein aggregates from the innocent bystanders. Annu Rev Neurosci 2003; 26:267–98.

    PubMed  CAS  Google Scholar 

  91. Fukutani Y, Cairns NJ, Shiozawa M, et al. Neuronal loss and neurofibrillary degeneration in the hippocampal cortex in late-onset sporadic Alzheimer’s disease. Psychiatry Clin Neurosci 2000; 54:523–9.

    PubMed  CAS  Google Scholar 

  92. Leuba G, Kraftsik R. Visual cortex in Alzheimer’s disease: occurrence of neuronal death and glial proliferation, and correlation with pathological hallmarks. Neurobiol Aging 1994; 15:29–43.

    PubMed  CAS  Google Scholar 

  93. Gomez-Isla T, Hollister R, West H, et al. Neuronal loss correlates with but exceeds neurofibrillary tangles in Alzheimer’s disease. Ann Neurol 1997; 41:17–24.

    PubMed  CAS  Google Scholar 

  94. Kril JJ, Patel S, Harding AJ, Halliday GM. Neuron loss from the hippocampus of Alzheimer’s disease exceeds extracellular neurofibrillary tangle formation. Acta Neuropathol (Berlin) 2002; 103:370–6.

    PubMed  Google Scholar 

  95. Bussiere T, Gold G, Kovari E, et al. Stereologic analysis of neurofibrillary tangle formation in prefrontal cortex area 9 in aging and Alzheimer’s disease. Neuroscience 2003; 117:577–92.

    PubMed  CAS  Google Scholar 

  96. Holness MJ, Langdown ML, Sugden MC. Earlylife programming of susceptibility to dysregulation of glucose metabolism and the development of Type 2 diabetes mellitus. Biochem J 2000; 349 Pt 3:657–65.

    PubMed  CAS  Google Scholar 

  97. David D, Hoerndli, F., Gotz, J. Functional Genomics meets neurodegenerative disorders Part I: Transcriptomic and proteomic technology. Prog Neurobiol 2005:1–16.

    Google Scholar 

  98. Hoerndli D, David, D., Gotz, J. Functional Genomics meets neurodegenerative disorders Part II: Transcriptomic and proteomic technology. Prog Neurobiol 2005:1–21.

    Google Scholar 

  99. Gotz J, Schild A, Hoerndli F, Pennanen L. Amyloid-induced neurofibrillary tangle formation in Alzheimer’s disease: Insight from transgenic mouse and tissue-culture models. Int J Dev Neurosci 2004; 22:453–65.

    PubMed  Google Scholar 

  100. Games D, Adams D, Alessandrini R, et al. Alzheimer-type neuropathology in transgenic mice overexpressing V717F beta-amyloid precursor protein [see comments]. Nature 1995; 373:523–7.

    PubMed  CAS  Google Scholar 

  101. Hsiao K, Chapman P, Nilsen S, et al. Correlative memory deficits, Abeta elevation, and amyloid plaques in transgenic mice [see comments]. Science 1996; 274:99–102.

    PubMed  CAS  Google Scholar 

  102. Sturchler-Pierrat C, Abramowski D, Duke M, et al. Two amyloid precursor protein transgenic mouse models with Alzheimer’s disease-like pathology. Proc Natl Acad Sci U S A 1997; 94:13287–92.

    PubMed  CAS  Google Scholar 

  103. Stalder M, Phinney A, Probst A, et al. Association of microglia with amyloid plaques in brains of APP23 transgenic mice. Am J Pathol 1999; 154:1673–84.

    PubMed  CAS  Google Scholar 

  104. Janus C, Pearson J, McLaurin J, et al. A beta peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer’s disease. Nature 2000; 408:979–82.

    PubMed  CAS  Google Scholar 

  105. Mucke L, Masliah E, Yu GQ, et al. High-level neuronal expression of abeta 1–42 in wild-type human amyloid protein precursor transgenic mice: Synaptotoxicity without plaque formation. J Neurosci 2000; 20:4050–8.

    PubMed  CAS  Google Scholar 

  106. Gotz J, Probst A, Spillantini MG, et al. Somatodendritic localization and hyperphosphorylation of tau protein in transgenic mice expressing the longest human brain tau isoform. EMBO J 1995; 14:1304–13.

    PubMed  CAS  Google Scholar 

  107. Ishihara T, Hong M, Zhang B, et al. Age-dependent emergence and progression of a tauopathy in transgenic mice overexpressing the shortest human tau isoform. Neuron 1999; 24:751–62.

    PubMed  CAS  Google Scholar 

  108. Spittaels K, Van den Haute C, Van Dorpe J, et al. Prominent axonopathy in the brain and spinal cord of transgenic mice overexpressing four-repeat human tau protein. Am J Pathol 1999; 155:2153–65.

    PubMed  CAS  Google Scholar 

  109. Probst A, Gotz J, Wiederhold KH, et al. Axonopathy and amyotrophy in mice transgenic for human four-repeat tau protein. Acta Neuropathol (Berlin) 2000; 99:469–81.

    PubMed  CAS  Google Scholar 

  110. Hirano A, Nakano I, Kurland LT, et al. Fine structural study of neurofibrillary changes in a family with amyotrophic lateral sclerosis. J Neuropathol Exp Neurol 1984; 43:471–80.

    PubMed  CAS  Google Scholar 

  111. Munoz DG, Greene C, Perl DP, Selkoe DJ. Accumulation of phosphorylated neurofilaments in anterior horn motoneurons of amyotrophic lateral sclerosis patients. J Neuropathol Exp Neurol 1988; 47:9–18.

    PubMed  CAS  Google Scholar 

  112. Rouleau GA, Clark AW, Rooke K, et al. SOD1 mutation is associated with accumulation of neurofilaments in amyotrophic lateral sclerosis. Ann Neurol 1996; 39:128–31.

    PubMed  CAS  Google Scholar 

  113. Ishihara T, Zhang B, Higuchi M, et al. Age-dependent induction of congophilic neurofibrillary tau inclusions in tau transgenic mice. Am J Pathol 2001; 158:555–62.

    PubMed  CAS  Google Scholar 

  114. Lewis J, McGowan E, Rockwood J, et al. Neurofibrillary tangles, amyotrophy and progressive motor disturbance in mice expressing mutant (P301L) tau protein. Nat Genet 2000; 25:402–5.

    PubMed  CAS  Google Scholar 

  115. Gotz J, Chen F, Barmettler R, Nitsch RM. Tau filament formation in transgenic mice expressing P301L tau. J Biol Chem 2001; 276:529–34.

    PubMed  CAS  Google Scholar 

  116. Tanemura K, Akagi T, Murayama M, et al. Formation of filamentous tau aggregations in transgenic mice expressing V337M human tau. Neurobiol Dis 2001; 8:1036–45.

    PubMed  CAS  Google Scholar 

  117. Tatebayashi Y, Miyasaka T, Chui DH, et al. Tau filament formation and associative memory deficit in aged mice expressing mutant (R406W) human tau. Proc Natl Acad Sci U S A 2002; 99:13896–901.

    PubMed  CAS  Google Scholar 

  118. Allen B, Ingram E, Takao M, et al. Abundant tau filaments and nonapoptotic neurodegeneration in transgenic mice expressing human P301S tau protein. J Neurosci 2002; 22:9340–51.

    PubMed  CAS  Google Scholar 

  119. Gotz J, Tolnay M, Barmettler R, et al. Oligodendroglial tau filament formation in transgenic mice expressing G272V tau. Eur J Neurosci 2001; 13:2131–40.

    PubMed  CAS  Google Scholar 

  120. Higuchi M, Ishihara T, Zhang B, et al. Transgenic mouse model of tauopathies with glial pathology and nervous system degeneration. Neuron 2002; 35:433–46.

    PubMed  CAS  Google Scholar 

  121. Oddo S, Caccamo A, Shepherd JD, et al. Tripletransgenic model of Alzheimer’s disease with plaques and tangles. Intracellular abeta and synaptic dysfunction. Neuron 2003; 39:409–21.

    PubMed  CAS  Google Scholar 

  122. Terwel D, Lasrado R, Snauwaert J, et al. Changed conformation of mutant Tau-P301L underlies the moribund tauopathy, absent in progressive, nonlethal axonopathy of Tau-4R/2N transgenic mice. J Biol Chem 2005; 280:3963–73.

    PubMed  CAS  Google Scholar 

  123. Sobrido MJ, Miller BL, Havlioglu N, et al. Novel tau polymorphisms, tau haplotypes, and splicing in familial and sporadic frontotemporal dementia. Arch Neurol 2003; 60:698–702.

    PubMed  Google Scholar 

  124. Gotz J, Chen F, van Dorpe J, Nitsch RM. Formation of neurofibrillary tangles in P301L tau transgenic mice induced by Abeta 42 fibrils. Science 2001; 293:1491–5.

    PubMed  CAS  Google Scholar 

  125. Santacruz K, Lewis J, Spires T, et al. Tau suppression in a neurodegenerative mouse model improves memory function. Science 2005; 309:476–81.

    PubMed  CAS  Google Scholar 

  126. Pennanen L, Welzl H, D’Adamo P, et al. Accelerated extinction of conditioned taste aversion in P301L tau transgenic mice. Neurobiol Dis 2004; 15:500–9.

    PubMed  CAS  Google Scholar 

  127. Pennanen L, Wolfer D, Nitsch RM, Gotz J. Impaired spatial reference memory in P301L tau transgenic mice. Genes, Brain and Behavior 2006; 5:369–379.

    CAS  Google Scholar 

  128. LeDoux JE. Emotion circuits in the brain. Annu Rev Neurosci 2000; 23:155–84.

    PubMed  CAS  Google Scholar 

  129. Welzl H, D’Adamo P, Lipp HP. Conditioned taste aversion as a learning and memory paradigm. Behav Brain Res 2001; 125:205–13.

    PubMed  CAS  Google Scholar 

  130. Tanemura K, Murayama M, Akagi T, et al. Neurodegeneration with tau accumulation in a transgenic mouse expressing V337M human tau. J Neurosci 2002; 22:133–41.

    PubMed  CAS  Google Scholar 

  131. Billings LM, Oddo S, Green KN, et al. Intraneuronal Abeta causes the onset of early Alzheimer’s disease-related cognitive deficits in transgenic mice. Neuron 2005; 45:675–88.

    PubMed  CAS  Google Scholar 

  132. Geula C, Wu CK, Saroff D, et al. Aging renders the brain vulnerable to amyloid beta-protein neurotoxicity [see comments]. Nat Med 1998; 4:827–31.

    PubMed  CAS  Google Scholar 

  133. Rapoport M, Dawson HN, Binder LI, et al. Tau is essential to beta-amyloid-induced neurotoxicity. Proc Natl Acad Sci U S A 2002; 99:6364–9.

    PubMed  CAS  Google Scholar 

  134. Lewis J, Dickson DW, Lin W-L, et al. Enhanced neurofibrillary degeneration in transgenic mice expressing mutant Tau and APP. Science 2001; 293:1487–91.

    PubMed  CAS  Google Scholar 

  135. Zirlinger M, Kreiman G, Anderson DJ. Amygdalaenriched genes identified by microarray technology are restricted to specific amygdaloid subnuclei. Proc Natl Acad Sci U S A 2001; 98:5270–5.

    PubMed  CAS  Google Scholar 

  136. Verdier Y, Penke B. Binding sites of amyloid betapeptide in cell plasma membrane and implications for Alzheimer’s disease. Curr Protein Pept Sci 2004; 5:19–31.

    PubMed  CAS  Google Scholar 

  137. Lashuel HA, Hartley D, Petre BM, et al. Neurodegenerative disease: amyloid pores from pathogenic mutations. Nature 2002; 418:291.

    PubMed  CAS  Google Scholar 

  138. Oddo S, Billings L, Kesslak JP, et al. Abeta immunotherapy leads to clearance of early, but not late, hyperphosphorylated tau aggregates via the proteasome. Neuron 2004; 43:321–32.

    PubMed  CAS  Google Scholar 

  139. David DC, Hauptmann S, Scherping I, et al. Proteomic and functional analysis reveal a mitochondrial dysfunction in P301L tau transgenic mice. J Biol Chem 2005; 280:23802–14.

    PubMed  CAS  Google Scholar 

  140. Keil U, Bonert A, Marques CA, et al. Amyloid betainduced changes in nitric oxide production and mitochondrial activity lead to apoptosis. J Biol Chem 2004; 279:50310–20.

    PubMed  CAS  Google Scholar 

  141. Sayre LM, Zelasko DA, Harris PL, et al. 4-Hydroxynonenal-derived advanced lipid peroxidation end products are increased in Alzheimer’s disease. J Neurochem 1997; 68:2092–7.

    Article  PubMed  CAS  Google Scholar 

  142. Perez M, Cuadros R, Smith MA, et al. Phosphorylated, but not native, tau protein assembles following reaction with the lipid peroxidation product, 4-hydroxy-2-nonenal. FEBS Lett 2000; 486:270–4.

    PubMed  CAS  Google Scholar 

  143. Takeda A, Smith MA, Avila J, et al. In Alzheimer’s disease, heme oxygenase is coincident with Alz50, an epitope of tau induced by 4-hydroxy-2-nonenal modification. J Neurochem 2000; 75:1234–41.

    PubMed  CAS  Google Scholar 

  144. Perez M, Hernandez F, Gomez-Ramos A, et al. Formation of aberrant phosphotau fibrillar polymers in neural cultured cells. Eur J Biochem 2002; 269:1484–9.

    PubMed  CAS  Google Scholar 

  145. Vogelsberg-Ragaglia V, Bruce J, Richter-Landsberg C, et al. Distinct FTDP-17 missense mutations in tau produce tau aggregates and other pathological phenotypes in transfected CHO cells. Mol Biol Cell 2000; 11:4093–104.

    PubMed  CAS  Google Scholar 

  146. Goldbaum O, Oppermann M, Handschuh M, et al. Proteasome inhibition stabilizes tau inclusions in oligodendroglial cells that occur after treatment with okadaic acid. J Neurosci 2003; 23:8872–80.

    PubMed  CAS  Google Scholar 

  147. Encinas M, Iglesias M, Liu Y, et al. Sequential treatment of SH-SY5Y cells with retinoic acid and brain-derived neurotrophic factor gives rise to fully differentiated, neurotrophic factor-dependent, human neuron-like cells. J Neurochem 2000; 75:991–1003.

    PubMed  CAS  Google Scholar 

  148. Ferrari A, Hoerndli F, Baechi T, et al. Beta-amyloid induces PHF-like tau filaments in tissue culture. J Biol Chem 2003; 278:40162–8.

    PubMed  CAS  Google Scholar 

  149. Abraha A, Ghoshal N, Gamblin TC, et al. C-terminal inhibition of tau assembly in vitro and in Alzheimer’s disease. J Cell Sci 2000; 113:3737–45.

    PubMed  CAS  Google Scholar 

  150. Fasulo L, Ugolini G, Visintin M, et al. The neuronal microtubule-associated protein tau is a substrate for caspase-3 and an effector of apoptosis. J Neurochem 2000; 75:624–33.

    PubMed  CAS  Google Scholar 

  151. Berry RW, Abraha A, Lagalwar S, et al. Inhibition of tau polymerization by its carboxy-terminal caspase cleavage fragment. Biochemistry 2003; 42:8325–31.

    PubMed  CAS  Google Scholar 

  152. Pennanen L, Gotz J. Different tau epitopes define Abeta(42)-mediated tau insolubility. Biochem Biophys Res Commun 2005; 337:1097–101.

    Article  PubMed  CAS  Google Scholar 

  153. Chen F, Wollmer MA, Hoerndli F, et al. Role for glyoxalase I in Alzheimer’s disease. Proc Natl Acad Sci U S A 2004; 101:7687–92.

    PubMed  CAS  Google Scholar 

  154. Brion JP, Tremp G, Octave JN. Transgenic expression of the shortest human tau affects its compartmentalization and its phosphorylation as in the pretangle stage of Alzheimer’s disease [see comments]. Am J Pathol 1999; 154:255–70.

    PubMed  CAS  Google Scholar 

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  1. Brain and Mind Research Institute (BMRI), University of Sydney, Camperdown, NSW, Australia

    Jürgen Götz PhD, Della C. David PhD & Lars M. Ittner MD

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Götz, J., David, D.C., Ittner, L.M. (2007). Impact of β-Amyloid on the Tau Pathology in Tau Transgenic Mouse and Tissue Culture Models. In: Barrow, C.J., Small, D.H. (eds) Abeta Peptide and Alzheimer’s Disease. Springer, London. https://doi.org/10.1007/978-1-84628-440-3_12

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